急性酒精处理小鼠中Xwak颗粒的化学成分及肝保护机制
Chemical Components and Hepatoprotective Mechanism of Xwak Granule in Mice Treated with Acute Alcohol.
作者信息
Chen Li, Liu Liu, Abdulla Rahima, Tursun Xirali, Xin Xuelei, Aisa Haji Akber
机构信息
Key Laboratory of Chemistry of Plant Resources in Arid Regions, State Key Laboratory Basis of Xinjiang Indigenous Medicinal Plants Resource Utilization, Xinjiang Technical Institute of Physics and Chemistry, Chinese Academy of Sciences, Urumqi 830011, China.
University of Chinese Academy of Sciences, Beijing 100049, China.
出版信息
Evid Based Complement Alternat Med. 2020 Sep 28;2020:8538474. doi: 10.1155/2020/8538474. eCollection 2020.
OBJECTIVE
To evaluate the hepatoprotective mechanism of Xwak granule (Xwak) in treatment of mice with alcoholic liver injury via activating ERK/NF-B and Nrf/HO-1 signaling pathways.
METHODS
The chemical composition of Xwak was tested by liquid chromatography coupled with mass spectrometry (LC-MS). Herein, 1,1-diphenyl-2-picrylhydrazyl (DPPH) scavenging assay and 2,2-azino-bis (3-ethylbenzothiazoline-6-sulphonic acid (ABTS) radical tests were performed . The hepatoprotective effect of Xwak was assessed at different concentrations (1.5, 3, and 6 g/kg) in a mouse model of alcoholic liver injury.
RESULTS
Totally, 48 compounds, including 16 flavonoids, 8 tannins, 9 chlorogenic acids, and 15 other compounds, were identified from Xwak. Xwak showed to have a satisfactory antioxidant activity . In a group of Xwak-treated mice, the serum levels of alanine transaminase (ALT), aspartate transaminase (AST), and alkaline phosphatase (ALP) were decreased compared with a group of the mouse model of alcoholic liver injury. In addition, the levels of antioxidant enzymes, such as glutathione peroxidase (GSH-PX), total superoxide dismutase (T-SOD), and catalase (CAT), were noticeably increased and the levels of malondialdehyde (MDA), tumor necrosis factor- (TNF-), transforming growth factor- (TGF-), and interleukin-6 (IL-6) were markedly reduced in the liver of mice. The state of oxidative stress in the mouse model of alcoholic liver injury was improved after treatment with Xwak. The improvement of inflammation-mediated disruption may conducive to the Xwak activity in the control of liver injury. The signals of p-ERK1/2, p-NF-B, COX-2, iNOS, CYP2E1, Nrf, and HO-1 were significantly induced in the liver of mice after treatment with Xwak.
CONCLUSIONS
The abovementioned findings indicated that the hepatoprotective mechanism of Xwak could be achieved by activating ERK/NF-B and Nrf/HO-1 signaling pathways to alleviate oxidative stress and inflammatory.
目的
通过激活ERK/NF-κB和Nrf/HO-1信号通路，评估醒脾颗粒（Xwak）对酒精性肝损伤小鼠的肝保护机制。
方法
采用液相色谱-质谱联用（LC-MS）法检测Xwak的化学成分。进行1,1-二苯基-2-苦基肼（DPPH）清除试验和2,2'-联氮-双-3-乙基苯并噻唑啉-6-磺酸（ABTS）自由基试验。在酒精性肝损伤小鼠模型中，评估不同浓度（1.5、3和6 g/kg）的Xwak的肝保护作用。
结果
从Xwak中总共鉴定出48种化合物，包括16种黄酮类、8种单宁类、9种绿原酸类和15种其他化合物。Xwak表现出令人满意的抗氧化活性。在一组经Xwak处理的小鼠中，与酒精性肝损伤小鼠模型组相比，血清丙氨酸转氨酶（ALT）、天冬氨酸转氨酶（AST）和碱性磷酸酶（ALP）水平降低。此外，小鼠肝脏中抗氧化酶如谷胱甘肽过氧化物酶（GSH-PX）、总超氧化物歧化酶（T-SOD）和过氧化氢酶（CAT）水平显著升高，丙二醛（MDA）、肿瘤坏死因子-α（TNF-α）、转化生长因子-β（TGF-β）和白细胞介素-6（IL-6）水平显著降低。经Xwak处理后，酒精性肝损伤小鼠模型的氧化应激状态得到改善。炎症介导的破坏的改善可能有助于Xwak在控制肝损伤中的活性。经Xwak处理后，小鼠肝脏中p-ERK1/2、p-NF-κB、COX-2、iNOS、CYP2E1、Nrf和HO-1的信号显著诱导。
结论
上述结果表明，Xwak的肝保护机制可能是通过激活ERK/NF-κB和Nrf/HO-1信号通路来减轻氧化应激和炎症。
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